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J Biol Chem. 2010 Apr 2;285(14):10832-40. doi: 10.1074/jbc.M109.091629. Epub 2010 Feb 4.

A conserved PMK-1/p38 MAPK is required in caenorhabditis elegans tissue-specific immune response to Yersinia pestis infection.

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Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.


Yersinia pestis has acquired a variety of complex strategies that enable the bacterium to overcome defenses in different hosts and ensure its survival and successful transmission. A full-genome microarray analysis on Caenorhabditis elegans infected with Y. pestis shows enrichment in genes that are markers of innate immune responses and regulated by a conserved PMK-1/p38 MAPK. Consistent with a role in regulating expression of immune effectors, inhibition of PMK-1/p38 by mutation or RNA interference enhances susceptibility to Y. pestis. Further studies of mosaic animals where PMK-1/p38 is exclusively inhibited or overexpressed in a tissue-specific manner indicate that PMK-1/p38 controls expression of a CUB-like family of immune genes at the cell-autonomous level. Given the conserved nature of PMK-1/p38 MAPK-mediated signaling and innate immune responses, PMK-1/p38 MAPK may play a role in the immune response against Y. pestis in natural hosts.

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